Cancer and Signalling: Targeting Cellular Pathways

A special issue of Biology (ISSN 2079-7737). This special issue belongs to the section "Cancer Biology".

Deadline for manuscript submissions: 15 May 2024 | Viewed by 2187

Special Issue Editor

Department of Biomolecular Sciences, Kingston University, Kingston upon Thames KT1 2EE, UK
Interests: Hippo signalling; mechanotransduction; YAP; cancer; polarity; Rho GTPases; signalling; organ growth; extracellular matrix; integrins
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Within all types of organisms there are fundamental cellular processes being orchestrated continuously in the background, resulting in the regulation of various signalling pathways. These pathways result in many cellular functions, including proliferation, cell–cell adhesion, extracellular matrix signalling, mechanotransduction, polarity and apoptosis, all of which are fundamental within cells. If these pathways dysfunction, then this can result in disease formation, including cancer. This Special Issue welcomes the submission of articles and reviews which cover a wide range of signalling pathways and examine how any disruption to these pathways can lead to cancer. I hope that we will try to expand upon what is currently known in the signalling field in this Special Issue by looking at new cutting-edge findings, which will hopefully shed some light on how signalling can control cancer progression, and possibly make us understand how we can combat this debilitating disease.

Dr. Ahmed Elbediwy
Guest Editor

Manuscript Submission Information

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Keywords

  • Hippo signalling
  • mechanotransduction
  • YAP
  • cancer
  • polarity
  • Rho GTPases
  • signalling, organ growth
  • extracellular matrix
  • integrins

Published Papers (1 paper)

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Review

50 pages, 8349 KiB  
Review
Expanding Roles of the E2F-RB-p53 Pathway in Tumor Suppression
by Yaxuan Zhou, Rinka Nakajima, Mashiro Shirasawa, Mariana Fikriyanti, Lin Zhao, Ritsuko Iwanaga, Andrew P. Bradford, Kenta Kurayoshi, Keigo Araki and Kiyoshi Ohtani
Biology 2023, 12(12), 1511; https://doi.org/10.3390/biology12121511 - 11 Dec 2023
Viewed by 1715
Abstract
The transcription factor E2F links the RB pathway to the p53 pathway upon loss of function of pRB, thereby playing a pivotal role in the suppression of tumorigenesis. E2F fulfills a major role in cell proliferation by controlling a variety of growth-associated genes. [...] Read more.
The transcription factor E2F links the RB pathway to the p53 pathway upon loss of function of pRB, thereby playing a pivotal role in the suppression of tumorigenesis. E2F fulfills a major role in cell proliferation by controlling a variety of growth-associated genes. The activity of E2F is controlled by the tumor suppressor pRB, which binds to E2F and actively suppresses target gene expression, thereby restraining cell proliferation. Signaling pathways originating from growth stimulative and growth suppressive signals converge on pRB (the RB pathway) to regulate E2F activity. In most cancers, the function of pRB is compromised by oncogenic mutations, and E2F activity is enhanced, thereby facilitating cell proliferation to promote tumorigenesis. Upon such events, E2F activates the Arf tumor suppressor gene, leading to activation of the tumor suppressor p53 to protect cells from tumorigenesis. ARF inactivates MDM2, which facilitates degradation of p53 through proteasome by ubiquitination (the p53 pathway). P53 suppresses tumorigenesis by inducing cellular senescence or apoptosis. Hence, in almost all cancers, the p53 pathway is also disabled. Here we will introduce the canonical functions of the RB-E2F-p53 pathway first and then the non-classical functions of each component, which may be relevant to cancer biology. Full article
(This article belongs to the Special Issue Cancer and Signalling: Targeting Cellular Pathways)
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Planned Papers

The below list represents only planned manuscripts. Some of these manuscripts have not been received by the Editorial Office yet. Papers submitted to MDPI journals are subject to peer-review.

Title: Drug repurposing and its effect on cancer signalling pathways
Authors: Natalia Haddad*; Sara Magura Gamaethige*; Nadine Wehida+; Ahmed Elbediwy+
Affiliation: Department of Biomolecular Sciences, Kingston University London, Kingston-upon-Thames KT1 2EE, UK
Abstract: The repurposing of clinically approved drugs as an alternative therapeutic approach to treating disease has gained significant attention in recent years. A multitude of research has demonstrated various and successful therapeutic interventions of these drugs in various neoplastic diseases, including multiple myeloma, leukemia, glioblastoma, and colon cancer. Drug repurposing has been widely encouraged due to the known efficacy, safety and convenience of these already established drugs, which allows the bypass of drug discovery and testing and provide existing (or established) safety profiles, thereby mitigating the failure of drugs at any of the complex steps during clinical trials. Repurposing drugs in cancer therapy is an exciting prospect due to the ability of these drugs to successfully target cancer-associated genes, often dysregulated in oncogenic signaling pathways, amongst which are the classical cancer signaling pathways WNT (wingless-related integration type) and Hippo signaling. These cancer signalling pathways play a fundamental role in controlling organ size, tissue homeostasis, cell proliferation, and apoptosis, all key hallmarks in cancer initiation and progression. Prolonged dysregulation of these pathways has been found to promote uncontrolled cellular growth and malignant transformation, contributing to carcinogenesis ultimately leading to malignancy. However, the translation of cancer signaling pathways and potential targeted therapies in cancer treatment faces ongoing challenges due to the pleiotropic nature of cancer cells, contributing to resistance and an increased rate of incomplete remission in patients. To address these challenges, several studies have suggested the approach of utilizing potential novel compounds including but not limited to N-arachidonoylethanolamine or Anandamide (AEA), an agonist of the endocannabinoid CB1 receptor, Chloroquine and artemisinin, successful and established antimalarial drugs, and a multitude of other categories of repurposed compounds treating such diseases as heart disease) incontinence, rheumatoid arthritis and anti-depressants. These non-oncological compounds have shown promising effectiveness in inhibiting tumor growth, proliferation, and migration by targeting key proteins associated with signaling networks such as WNT and Hippo signaling pathways. This review provides analysis of a range of potential cancer compounds in drug repurposing. It unravels the current understanding of the molecular rationale for repurposing these drugs and their potential in targeting key oncogenic signaling pathways, while also highlighting the challenges associated with their translation into effective cancer treatments.

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